It is highly desirable to reliably track respiration within patients having pacemakers and ICDs. Tracking patient respiration permits potentially dangerous respiratory disorders, such as apnea, hypopnea, hyperpnea, nocturnal asthma, and Cheyne-Stokes Respiration (CSR), to be detected. Apnea and hypopnea are abnormal respiration patterns characterized by periods of significantly reduced respiration. With hypopnea, respiration is reduced but still present. With apnea, however, respiration may cease completely for 10 seconds or longer. One common form of apnea is central sleep apnea (CSA), which appears to arise during sleep due to a neurological defect. Another form of apnea is obstructive sleep apnea (OSA), which arises due to obstruction of the respiratory pathways during sleep. Patients with sleep apnea experience frequent wakefulness at night and excessive sleepiness during the day. In addition, apnea can exacerbate various medical conditions, particularly hypertension. Apnea can also exacerbate congestive heart failure (CHF), a condition wherein the patient suffers from poor cardiac function. Indeed, the aberrant blood chemistry levels occurring during sleep apnea are a significant problem for patients with CHF. Due to poor cardiac function caused by CHF, patients already suffer from generally low blood oxygen levels. Frequent periods of sleep apnea result in even lower blood oxygen levels.
Episodes of apnea can also occur during CSR, which is an abnormal respiratory pattern often occurring in patients with CHF. CSR is characterized by alternating periods of hypopnea and hyperpnea (i.e. fast, deep breathing.) Briefly, CSR arises principally due to a time lag between blood CO2 levels sensed by the respiratory control nerve centers of the brain and the blood CO2 levels. With CHF, poor cardiac function results in poor blood flow to the brain such that respiratory control nerve centers respond to blood CO2 levels that are no longer properly representative of the overall blood CO2 levels in the body. Hence, the respiratory control nerve centers trigger an increase in the depth and frequency of breathing in an attempt to compensate for perceived high blood CO2 levels—although the blood CO2 levels have already dropped. By the time the respiratory control nerve centers detect the drop in blood CO2 levels and act to slow respiration, the blood CO2 levels have already increased. This cycle becomes increasingly unbalanced until respiration alternates between hypopnea and hyperpnea. The periods of hypopnea often become sufficiently severe that no breathing occurs between the periods of hyperpnea, i.e. periods of frank apnea occur between the periods of hyperpnea. The wildly fluctuating blood chemistry levels caused by alternating between hyperpnea and apnea/hypopnea can significantly exacerbate CHF and other medical conditions. When CHF is still mild, CSR usually occurs, if at all, only while the patient is sleeping. When it becomes more severe, CSR can occur while the patient is awake.
Abnormal respiration during sleep may also arise due to nocturnal asthma. With asthma, the linings of the airways swell and become more inflamed. Mucus clogs the airways and the muscles around the airways tighten and narrow. Hence, breathing becomes difficult and stressful. During an asthma attack, rapid breathing patterns similar to hyperpnea occur, though little or no oxygen actual reaches the lungs. An asthma attack may be triggered by allergens, respiratory infections, cold and dry air, or even heartburn. The majority of asthma attacks occur during the night, between 3:00 a.m. and 5:00 a.m. Nocturnal asthma has been associated with factors such as decreased pulmonary function, hypoxemia and circadian variations of histamine, epinephrine, and cortisol concentrations. Asthma attacks at night may also be triggered directly by sleep apnea. Nocturnal asthma attacks may be fatal, particularly within patients also suffering from CHF.
In view of the significant adverse consequences of apnea/hypopnea, nocturnal asthma, or CSR, particularly insofar as patients with CHF are concerned, it is highly desirable to provide techniques for detecting such conditions. Tracking actual patient respiration provides perhaps the most direct and effective technique for detecting respiratory disorders. For patients with pacemakers and ICDs, respiration is conventionally tracked based on thoracic impedance as measured via pacing/sensing leads implanted within the heart. Sensing of the intracardiac electrogram (IEGM) of the patient is temporarily suspended during each cardiac cycle so as to sense an impedance signal, from which respiration patterns are derived. See, for example, U.S. Pat. No. 6,449,509 to Park, et al., entitled “Implantable Stimulation Device Having Synchronous Sampling for a Respiration Sensor.”
Although impedance-based techniques are useful, it would be desirable to provide alternative techniques for tracking respiration, particularly for the purposes of detecting episodes of abnormal respiration, wherein respiration is derived solely from the IEGM signal so as to eliminate the need to detect or process impedance. Additionally, this eliminates need for additional sensors, and the sensing electrodes can be thus used for IEGM based breathing pattern detection and hence, the ease of implementability in current platforms. One technique for deriving respiration from an IEGM signal is set forth in U.S. Pat. No. 6,697,672 to Andersson, entitled “Implantable Heart Stimulator”, which is incorporated by reference herein. Briefly, Andersson provides a technique to extract parameters related to patient respiration from an analysis of intervals between various events detected within a ventricular-IEGM (i.e. V-IEGM) signal. For example, cycle-to-cycle variability is tracked in R-R intervals or in the amplitude of S-T intervals. In other words, the technique of Andersson exploits interval-based morphological features of the V-IEGM to track respiration. Although not discussed in the Andersson reference, autonomic variability arising during respiration causes the interval-based changes in the IEGM. R-waves (also referred to as QRS-complexes) are electrical signals representative of the depolarization of ventricular muscle tissue. The subsequent electrical repolarization of the ventricular tissue appears within the IEGM as a T-wave. Electrical depolarization of atrial muscle tissue is manifest as a P-wave. Strictly speaking, P-waves, R-waves and T-waves are features of a surface electrocardiogram (EKG or ECG). For convenience, the terms P-wave, R-wave and T-wave are also used herein (and in the literature) to refer to the corresponding internal signal component.
Although the interval-based variability technique of Andersson is effective, it is desirable to provide additional or alternative IEGM-based techniques for trending and tracking respiration and for detecting episodes of abnormal respiration. This general goal was achieved by the techniques of patent application Ser. No. 11/127,389, cited above. Briefly, respiration patterns are detected based upon cycle-to-cycle changes in morphological features associated with individual electrical events with the IEGM signals. For example, slight changes in the peak amplitudes of QRS-complexes, P-waves or T-waves are tracked to identify cyclical variations representative of patient respiration. Alternatively, the integrals of the morphological features of the individual events may be calculated for use in tracking respiration. Once respiration patterns have been identified, episodes of abnormal respiration, such as apnea, hyperpnea, nocturnal asthma, or the like, may be detected and therapy automatically delivered.
Hence, the techniques of patent application Ser. No. 11/127,389, which are also described herein below, are not limited to analyzing interval-based features of a V-IEGM, as with certain predecessor techniques. Instead, the techniques of the parent application examine changes within individual features of cardiac cycles over time. In this regard, it has been observed that respiration causes slight variations in the size and shape of individual electrical events of the IEGM signals, such as QRS-complexes, and that those changes are correlated with respiration. This differs from changes in intervals (such as R-R intervals), which, as noted, appear to arise due to autonomic variability. In one specific example, changes in the integrals of the QRS-complex derived from a V-IEGM channel signal are examined, alone or in combination with, integrals of P-waves derived from an atrial IEGM (A-IEGM) channel signal. Interval-based parameters, such as variations in A-A, R-R or AV intervals, may be additionally used to aid in tracking respiration but are not required. That predecessor application also presented techniques for detecting episodes of abnormal respiration based on respiration patterns derived from IEGMs, such as episodes of such as apnea, hypopnea, nocturnal asthma, or CSR.
Patent application Ser. No. 11/416,317 provided further improvements in the area of abnormal respiration detection based on IEGM signals. These improvements, which are also described herein below, are particularly directed to exploiting respiratory parameters such as inter-breath interval, respiration depth, and respiration power in the detection of abnormal respiration, with each of the respiratory parameters conveniently derived from IEGM signals. These techniques are particularly well suited to detecting episodes of abnormal respiration during sleep. In this regard, normal respiration during sleep is characterized by an almost constant respiration depth (corrected for patient posture and other non-respiratory factors). Hence, significant changes in respiration depth or other parameters associated with the respiratory cycles are indicative of a transition from normal respiration to some form of abnormal respiration. Further analysis of the respiratory parameters is used to identify the particular form of abnormal respiration. The technique can also be used to track and trend sleep disorder breathing or, in general, disordered breathing. Depending upon the capabilities of the implanted device, appropriate therapy may then be delivered. For example, an alarm device may be triggered to alert the patient upon detection of an episode of apnea/hypopnea. The alarm device may be, e.g., an implanted device such as a “tickle” voltage warning device or a bedside warning system that emits an audible alarm. In this manner, if the patient is asleep, the patient is thereby awakened so as to prevent extended episodes of apnea/hypopnea from occurring, which can cause significant variances in blood chemistry that can exacerbate other medical conditions such as CHF.
Although the techniques of the predecessor applications cited above are quite useful, room for still further improvement remains. In particular, it would be desirable to exploit pattern classifiers (such as pattern classifiers of the type described in U.S. Pat. No. 7,025,729 to de Chazal, et al., entitled “Apparatus for Detecting Sleep Apnea using Electrocardiogram Signals”) to discriminate normal and abnormal respiration based on IEGM signals detected by an implantable medical device. It would also be desirable to evaluate the severity of abnormal respiration within a patient and to further discriminate different types of abnormal respiration, such as to discriminate CSA from OSA. Accordingly, various aspects of the present invention are directed to these ends.